Disturbances of the redox state of the B cell may be involved in the pathogenesis of B cell viability and anomalies in insulin release observed in diabetes. The diabetogenic agents streptozotocin and alloxan appear to cause irreversible changes in the redox state of the B cell which lead to cell damage. Small changes in the redox state of the B cell by sulfhydryl agents modify insulin release. The present study intends to further define the mechanisms through which redox changes occur in the B cell and the effect of these changes on cell viability and insulin release. Firstly, the effects of streptozotocin and alloxan on B cell viability are to be assessed by changes in the reduced to oxidized glutathione ratio, changes in the ratio of reduced to oxidized pyridine nucleotides, on the production of free radicals, and on the effect of these agents on the activity of the hexose monophosphate shunt. Second to assess the effect of small changes in the B cell redox state on insulin release brought about by low concentrations of oxidant or sulfhydryl agents. Third to characterize the acute metabolic events following M. strain EMC virus induced diabetes in mice, and to assess whether this virus induces changes in the redox state of cells.